CAJ | 학술논문

目的：探讨蛋白激酶B（protein kinase B，Akt）抑制剂MK－2206对胃癌细胞SGC－7901DNA损伤的影响。方法：不同浓度的MK－2206作用于SGC－7901细胞后，免疫荧光检测细胞内DNA损伤标记分子磷酸化组蛋白H2AX（γ－H2AX）焦点的生成，Western blot检测DNA损伤相关蛋白的表达水平，同时观察MK－2206对自噬标志蛋白LC3－II表达量的影响，用以确定MK－2206是否促进细胞发生自噬。结果： MK－2206能够诱导SGC－7901细胞发生DNA损伤，促进细胞内γ－H2AX焦点生成，并且激活DNA损伤相关蛋白的表达；MK－2206作用细胞后，LC3－II的生成增加；抑制细胞的自噬显著增强了MK－2206诱导的H2AX磷酸化水平。结论： Akt抑制剂MK－2206能够诱导细胞发生DNA损伤和自噬，抑制自噬促进了MK－2206诱导的DNA损伤。
목적：탐토단백격매B（protein kinase B，Akt）억제제MK－2206대위암세포SGC－7901DNA손상적영향。방법：불동농도적MK－2206작용우SGC－7901세포후，면역형광검측세포내DNA손상표기분자린산화조단백H2AX（γ－H2AX）초점적생성，Western blot검측DNA손상상관단백적표체수평，동시관찰MK－2206대자서표지단백LC3－II표체량적영향，용이학정MK－2206시부촉진세포발생자서。결과： MK－2206능구유도SGC－7901세포발생DNA손상，촉진세포내γ－H2AX초점생성，병차격활DNA손상상관단백적표체；MK－2206작용세포후，LC3－II적생성증가；억제세포적자서현저증강료MK－2206유도적H2AX린산화수평。결론： Akt억제제MK－2206능구유도세포발생DNA손상화자서，억제자서촉진료MK－2206유도적DNA손상。
AIM:To investigate the effect of MK-2206, an inhibitor of protein kinase B (Akt), on the DNA damage of SGC-7901 cells.METHODS: SGC-7901 cells were treated with different concentrations of MK-2206, and phosphorylated histone H2AX (γ-H2AX) foci formation was detected by immunofluorescence staining .Western blot analy-sis was used to exam the levels of DNA damage-related protein.The expression of LC3-Ⅱ was determined to evaluate the change of autophagy .RESULTS:MK-2206 treatment increased the formation of γ-H2AX foci and histone H2AX phospho-rylation in the SGC-7901 cells.The levels of DNA damage response protein were also increased .In addition, MK-2206-treated SGC-7901 cells increased the expression of LC 3-II, a hallmark of autophagy .Inhibition of autophagy significantly enhanced MK-2206-mediated histone H2AX phosphorylation.CONCLUSION:MK-2206 induces DNA damage and auto-phagy in SGC-7901 cells.Blocking autophagy potentiates the response of MK-2206-induced DNA damage .